Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P17174 (
aspartate aminotransferase
)
14,872
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
We examined the sensitivity of metallothionein (MT)-III null mice to cadmium (Cd)-induced acute hepatotoxicity. MT-I/II null mice were also used to compare Cd toxicities between
MT-III
null mice and MT-I/II null mice. Male MT-I/II null mice,
MT-III
null mice and wild-type mice were given s.c. injection of Cd (5-20 micromol/kg) and then the blood and liver were collected from each mouse under ether anesthesia at 2 days after the administration. Serum alanine aminotransferase (ALT) and
aspartate aminotransferase
(
AST
) activities elevated by injection of Cd were significantly higher in the MT-I/II null mice than in the wild-type mice. In the
MT-III
null mice, ALT and
AST
activities were not elevated following the injection of Cd. Further, marked morphological changes such as necrosis of hepatocytes, severe hemorrhage and congestion were observed by injection of Cd in both MT-I/II null mice and wild-type mice, whereas the degree of injury was found to be more extensive in MT-I/II null mice. In contrast, only occasional damage was observed in the liver of
MT-III
null mice treated with the same dose of Cd. These morphological observations were consistent with the results of ALT and
AST
activities. In the present study, it was clearly found that
MT-III
null mice were resistant to Cd hepatotoxicity, although MT-I/II null mice were sensitive to its toxicity.
MT-III
may be an accelerative factor in Cd-induced acute hepatotoxicity.
...
PMID:Resistance of metallothionein-III null mice to cadmium-induced acute hepatotoxicity. 2037 71